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Patients with OSA show exaggerated sympathetic tone, leading to hypertension, cardiac arrhythmia, profuse sweating, impaired cerebral perfusion, and stroke. In addition, OSA appears in 86% of obese Type II diabetic patients, suggesting common deleterious processes. Autonomic deficiencies also appear in CCHS patients, who are often hypoglycemic. The impaired autonomic control may stem from injury to central sympathetic and parasympathetic regulatory areas resulting from apnea\u2010related inflammation, hypoxia, or perfusion\u2010related consequences in OSA, and genetic mutation repercussions in CCHS. Disturbed sleep organization from apnea arousals may also disrupt hormonal release. Brain areas affected in both OSA and CCHS include cortical and limbic regions that influence hypothalamic\u2010regulated sympathetic control and hormone release, essential for glycemic regulation, as well as parasympathetic nuclei influencing the pancreas and other viscera, and raph\u00e9 serotonergic sites, important for thermal and vascular regulation. Brain injury and altered functional responses appear in OSA and CCHS, assessed with magnetic resonance imaging techniques, in areas which show regional gray matter loss, alterations of free water within tissue, loss of axonal integrity, and disruption of functional responses to autonomic and ventilatory challenges. Evaluation of neural injury and distortion in functional signals to autonomic challenges in localized brain areas can provide insights into common pathological mechanisms for dysregulation of hormonal release and autonomic processes in sleep\u2010disordered breathing and metabolic disorders. 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